A kinematic analysis of the instant centers of rotation analysis was performed on 21 metacarpophalangeal joints from 11 horses. Manual and computerized methods were used to locate the instant center of rotation on photocopies of transparent composite tracings of a series of radiographs of each joint. The instant centers of rotation of the proximal phalanx about the distal portion of the third metacarpal bone were located consistently on or near the eminence for attachment of the collateral ligaments. The instant centers of rotation of the sesamoids about the distal portion of the third metacarpal bone were consistently located near the dorsal articular margin of the distal portion of the third metacarpal bone. Rotation of the joint as it extended caused minor variation in radiographic projection. This variation in radiographic projection limited the precision of the analysis of the instant center of rotation and prevented the identification of a single instant center of rotation or an instant center of rotation pathway for the articulation of the proximal phalanx or the proximal sesamoids with the distal portion of the third metacarpal bone. The articular surface velocity vectors determined from the instant centers of rotation indicated that the joint surfaces slide on each other. The motion of the joint caused compression at the dorsal articular margins at maximal extension and thereby limited further extension. At this degree of extension, the proximal sesamoidsarticulated only with the proximal sesamoid-metacarpal articular surface of the distal portion of the third metacarpal bone.

During initial studies, we found that many fluorescein isothiocyanate-labeled anti-immunoglobulin conjugates were unstable and tended to aggregate and precipitate when used for indirect immunofluorescence microscopy. In some instances, the precipitate was extensive enough to interfere with interpretation of the test results. Attempts to resolve this problem resulted in a procedure by which such conjugates were digested with papain to Fab and Fc fragments before use. Aggregation and precipitation were prevented, while desired antibody activity was retained. Digestion with papain also reduced the diffuse background fluorescence (commonly referred to as nonspecific fluorescence or staining) that is often associated with conjugates before they are sorbed with tissue powders or chromatographed to remove highly labeled immunoglobulin molecules.

Fifty-five horses were inoculated IV and/or SC with materials containing Ehrlichia risticii, ie, infected whole blood, buffy coat cells, or cell culture, to study clinical and hematologic features of equine monocytic ehrlichiosis (Potomac horse fever). Major clinical and hematologic features of induced E risticii infection were biphasic increase in rectal temperature with peak increases of 38.9 C and 39.3 C on postinoculation days (PID) 5 and 12, respectively; depression; anorexia; decreased WBC count (maximal decrease of 47% on PID 12); and diarrhea from PID 14 to PID 18. Increased WBC count was an inconsistent feature, with a maximal increase of 51.5% on PID 20. During times of decreased and increased WBC counts, lymphocyte/neutrophil ratios remained fairly constant. However, not all horses had all clinical and hematologic features, and these features were present in different degrees among horses. Increased rectal temperature, depression, anorexia, and decreased WBC count were more consistent features, whereas diarrhea developed in 73% of the horses. Of 55 horses, 39 (71%) had all clinical and hematologic features of the disease (classic disease), whereas 16 (29%) horses did not have greater than or equal to 1 of these features (nonclassic disease). The E risticii titer in the blood (ehrlichemia) was maximum during the peak increase in rectal temperature. In 55 horses, mortality was 9%. Significant differences (P > 0.5) in clinical and hematologic features were not detected between horses that survived and those that died of E risticii infection.

Twelve Holstein calves mere used to determine the prophylactic efficacy of ivermectin against challenge exposure with gastrointestinal and pulmonary nematodes. Two groups of 6 calves (mean body weight, 205 kg) each were formed by restricted randomization according to body weight. Group-l calves served as nonmedicated controls. Each calf of group 2 was orally given one prototype sustained-release bolus designed to deliver ivermectin at a continuous daily dose of 8 mg. Third-stage nematode infective larvae were given to the calves on posttreatment days 28 and 42. The calves were euthanatized 77 or 78 days after treatment. Ivermectin was 100% effective (P < 0.05) in preventing the establishment of infection by Haemonchus placei, Ostertagia ostertagi, Cooperia spp (C punctata, C oncophora, C surnabada), Nematodirus helvetianus, Oesophagostomum radiatum, and Dictyocaulus viviparus and was > 99% effective against Trichostrongylus axei. Incidental infection by Trichuris spp was reduced by 94% (P = 0.08).

Hybridomas were selected for secretion of monoclonal antibodies directed against pseudorabies virus (PRV) glycoproteins. Each monoclonal antibody was capable of neutralizing PRV in vitro in the presence of complement. This panel of antibodies was used in passive immunization studies to protect mice and swine from PRV-induced mortality. The most protective antibody in mice was 3A4, specific for PRV glycoprotein gp50, which afforded as high as 100% protection. Although antibody 3A4 was partially protective in swine, antibody 3D11, which is specific for PRV glycoprotein gIII, afforded greater protection-83% protection when ascitic fluid was used and 100% protection when immunoglobulin concentrated from cell cultures was used at a dose of 150 mg/pig. These studies demonstrated that monoclonal antibodies may be useful for short-term prophylaxis against PRV-induced disease and that antibody directed against either PRV gylcoprotein gIII or gp50 is sufficient to protect animals from PRV-induced mortality.

A specialized tip structure in some mycoplasmas facilitates their attachment to host cells. Mycoplasma bovoculi strains FS8-7 and M165/69 did not have specialized membrane structure and did not exhibit capsule when stained with ruthenium red and examined by use of transmission electron microscopy. The organisms attached in vitro to bovine lung fibroblasts, with no apparent specialized structure. Attachment to conjunctival epithelium in vivo was observed (after death) in a calf infected with M bovoculi. Close association between M bovoculi and the host cells was noticed. Mycoplasmal cells pretreated with hyperimmune rabbit serum and labeled with protein A-gold complex had gold particles randomly distributed around the membrane. Gold-labeled monoclonal antibodies, M25.5 and M7.3, which were directed against 2 surface antigens of M bovoculi, also were distributed randomly on the mycoplasmal surface as seen in results of double-labeling experiments.

Adherence of Streptococcus dysgalactiae isolates from cattle and S equi isolates from horses to their respective host epithelial cells was compared with the adherence of S pyogenes to human epithelial cells. The adherence was quantitatively determined by use of fluorescein-labeled streptococci. All 3 streptococcal species adhered selectively to their respective host cells. The mechanism of adherence was evaluated by binding studies with adhesive plasma protein, fibronectin. Although all 3 streptococcal species bound fibronectin, S dysgalactiae and S equi interacted preferentially with a 210-kilodalton (kD) C-terminal fragment of fibronectin, whereas S pyogenes bound only a 29-kD N-terminal fragment. A synthetic peptide Gly-Arg-Gly-Asp-Ser, representing the host cell attachment site of fibronectin, partially inhibited the binding of fibronectin and of its 210 kD fragment to S dysgalactiae, but not to S equi. The binding of fibronectin and its 29-kD fragment to S pyogenes was not inhibited by Gly-Arg-Gly-Asp-Ser. These differences in binding activities corresponded to the ability of fibronectin to mediate the adherence of the streptococci to the epithelial cells: fibronectin strongly inhibited the adherence of S pyogenes and S equi to the epithelial cells, but only weakly inhibited that of S dysgalactiae.

Two techniques for end-to-end anastomosis of the small colon were evaluated in each of 6 horses. A simple interrupted suture pattern that excluded the mucosa and was oversewn with an inverting suture was compared with a triangulated double-row pattern of stainless steel staples. Anastomotic sites were evaluated at 2 weeks, 2 months, and 6 months for extent of abdominal adhesions, lumen diameter at anastomotic sites, bursting pressures, and healing response. Clinical postoperative complications were not associated with either technique. At postmortem examination, there was extensive adhesion formation from the mesocolon to the stapled anastomotic site. The suture technique resulted in greater luminal diameters (P less than or equal to 0.05), with good apposition of the tissue layers. Staples were missing as early as 2 weeks after surgery, and their loss was associated with separation of the muscularis at later evaluation periods. Regardless of technique, all but one anastomotic segment burst away from the anastomotic site along the mesenteric taenial band. For the 12 anastomoses performed in normal horses, the suturing technique was better than the stapling technique because of significantly larger lumen diameters, better anastomotic healing, and minimal intra-abdominal adhesion formation.

Lymphocytes from 5 clinically normal lambs and 5 lambs affected with ovine hereditary chondrodysplasia (spider syndrome) were cultured, G-banded, and karyotyped. Fifty metaphase karyotypes and one heterogram were evaluated for chromosome number and morphologic features. All lambs had normal diploid (2n) chromosome numbers of 54,XX or 54,XY, and there were no apparent differences in the morphologic features of the chromosomes.

Morphologic changes developing during bovine mammary involution were examined. Quarter biopsy specimens were obtained weekly from 5 cows beginning the day milking was discontinued through parturition. Light and electron microscopic examination of mammary tissue indicated a gradual reduction in synthetic and secretory activity of alveolar epithelium as involution progressed. Light microscopic morphologic analysis revealed increases in stroma and nonactive secretory epithelium, with concomitant decreases in epithelium, lumen, and fully active secretory epithelium during the first 2 weeks of involution. Electron microscopic analysis of alveolar epithelium revealed decreased number of organelles associated with milk synthesis and secretion during this time. These changes reversed gradually beginning 2 weeks before parturition, and by the time of calving, cell structure was typical of lactating glands. Tissue from infected quarters had less synthetic and secretory ability as indicated by significantly higher percentages of stroma and nonactive cells, but lower percentages of lumen and moderately active cells, compared with uninfected quarters. Infected quarters also had more leukocytes infiltrating the epithelium, lumen, and stroma, compared with uninfected quarters. Microscopic examination of macrophages and neutrophils suggested these cells removed milk components and cellular debris during involution. Large numbers of plasma cells, with distended cisternae of rough endoplasmic reticulum, suggested local antibody production during the periparturient period.